Gingivitis

Gingivitis is an inflammatory process limited to the mucosal epithelial tissue surrounding the cervical portion of the teeth and the alveolar processes. Gingivitis has been classified by clinical appearance (eg, ulcerative, hemorrhagic, necrotizing, purulent), etiology (eg, drug-induced, hormonal, nutritional, infectious, plaque-induced), and duration (acute, chronic). The most common type of gingivitis is a chronic form induced by plaque. Gingivitis is shown in the image below.

During the global COVID-19 pandemic, many patients found it difficult to access preventive dental care. This has increased the number of people at risk for poor oral health, especially among those of lower socioeconomic status.[1]

Compare the image above to a healthy mouth, below.

Acute necrotizing ulcerative gingivitis (ANUG, ie, trench mouth) is an acute infectious gingivitis. The term trench mouth was coined in World War I when ANUG was common among trench-bound soldiers.

The most common type of gingivitis involves the marginal gingiva and is brought on by the accumulation of microbial plaques in persons with inadequate oral hygiene. Gingivitis proceeds through an initial stage to produce early lesions, which then progress to advanced disease.

The initial stage of an acute exudative inflammatory response begins within 4 or 5 days of plaque accumulation. Both gingival fluid and transmigration of neutrophils increase. Deposition of fibrin and destruction of collagen can be noted in the initial stage. At approximately 1 week, transition to early lesions is marked by the change to predominately lymphocytic infiltrates. Monocytes and plasma cells also may be present. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. As chronic local inflammation progresses, pockets develop where the gingiva separates from the tooth. These pockets deepen and may bleed during tooth brushing, flossing, and even normal chewing. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Teeth loosen and eventually fall out.

ANUG is a completely different syndrome caused by acute infection of the gingiva with organisms such as Prevotella intermedia, alpha-hemolytic streptococci, Actinomyces species, or any of a number of different oral spirochetes. ANUG may result in accelerated destruction of affected tissues, as well as local or systemic spread of infection.

Noma (cancrum oris) is a syndrome in which ANUG spreads beyond the gingiva. The infection invades local tissues of the mouth and face.

Although bacteria play a role in all forms of gingivitis, the primary cause of chronic gingivitis is inadequate oral hygiene.

Risk factors

Use of tobacco or ethanol is thought to be a risk factor.

Immune incompetence is observed more frequently in HIV-infected children. As their CD4 counts decline, incidence of gingivitis may increase. Diabetes mellitus increases the risk of gingivitis and periodontitis.

Drug-induced causes

The list of drugs that cause gingivitis and gingival bleeding is extensive.

Gingival bleeding may occur with the use of anticoagulants and fibrinolytic agents.

Phenytoin, oral contraceptive agents, and calcium channel blockers may cause gingival hyperplasia.

Gingivitis has been observed with use of protease inhibitors (eg, saquinavir, ritonavir), vitamin A and analogues, danazol, pentamidine, misoprostol, methotrexate, and gold compounds.

Gingivostomatitis has been observed in exposure to arsenic, gold, bismuth, mercury, nickel, sulfur dioxide, lead, thallium, zinc, methyl violet, and topical chlorhexidine.

Acute necrotizing ulcerative gingivitis

Acute necrotizing infection may occur as a complication of chronic gingivitis in situations in which hygiene is abandoned completely or host defenses are weakened.

ANUG is the result of soft tissue invasion by ubiquitous organisms and is not believed to be contagious. It is a risk wherever poor sanitation, diet, or oral hygiene is present. Living near livestock is an additional risk factor.

Other causes

Other causes include the following:

• Inadequate plaque removal

• Blood dyscrasias

• Allergic reactions

• Chronic debilitating disease

• Poor nutrition

• Lack of periodic dental examinations

United States statistics

Frequency is difficult to determine because of the lack of agreement on measurement criteria. Many people believe that gingivitis begins in early childhood and that 9-17% of children aged 3-11 years have gingivitis. At puberty, prevalence rises to 70-90%. In recent years, periodontal disease, the endpoint of chronic gingivitis, slowly has decreased among adult Americans. However, chronic periodontitis is still the most prevalent chronic inflammatory condition in the elderly.[2]

ANUG may be a clinical problem in immunocompromised patients during chemotherapy. Gingivitis and resulting periodontal disease are seen more frequently in patients with either diabetes or HIV infection.

International statistics

Studies in Australia, Sweden, England, and Switzerland report gingivitis in 48-85% of children aged 3-6 years, but whether this range reflects population differences or whether it is due to different criteria used to define the disease is difficult to know. In adolescence, incidence around the world is comparable to US data (70-90%). ANUG may be found in areas where those at risk, particularly children, face poor living conditions. More recent publications show several cases in areas such as Nigeria, where ANUG and noma were observed in children younger than 14 years.[3]

Sex- and age-related demographics

Gingivitis is slightly more prevalent in males than in females because females tend to have better oral hygiene.

Adults are most commonly affected.

Children from sub-Saharan regions of Africa may be at risk for ANUG because of poor living conditions.

Untreated chronic gingivitis eventually results in tooth loss. After an initial cleaning and scaling in its early stages, gingivitis usually is reversible with good dental hygiene. Gingivitis generally responds well to appropriate treatment.

ANUG responds to treatment if host defenses are intact. Noma requires aggressive treatment with antibiotics and local debridement. The usual course is acute, relapsing, intermittent, and chronic.

Morbidity/mortality

Periodontal disease has been shown in some studies to be an associated factor in coronary artery disease (CAD) and cerebrovascular disease/ischemic stroke.[4, 5, 6, 7]  Elevated levels of chronic inflammation (eg, C-reactive protein) have been shown to fall after treatment of periodontal disease. These elevated markers have clear association with vascular disease, so treatment of periodontal disease may theoretically have an impact on CAD and ischemic CNS disease.[8]  However, a clear cause-and-effect relationship has not been demonstrated between treatment of periodontal disease and improvement of atherosclerotic diseases or outcomes.[9]  A study that induced gingivitis in healthy volunteers was associated with a clear increase in inflammatory markers.[10]

A study by Sen et al that included data from 10,362 stroke-free participants, and 584 participants that had incident ischemic strokes over a 15-year period reported that periodontal disease was associated with cardioembolic (hazard ratio, 2.6; 95% confidence interval, 1.2-5.6) and thrombotic (hazard ratio, 2.2; 95% confidence interval, 1.3-3.8) stroke subtypes. The study also added that a lower stroke risk was associated with regular dental care utilization (hazard ratio, 0.77; 95% confidence interval, 0.63-0.94).[11]

A large study that enrolled 805 patients with a first myocardial infarction (MI) and 805 control patients without MI concluded that the risk of a first myocardial infarction was significantly increased in patients with periodontitis. The study found that 43% of MI patients vs 33% of matched controls had mild to severe periodontitis. After researchers controlled for smoking, diabetes, education, and marital status, individuals with periodontitis had a 28% increased risk of MI.[12, 13]

Periodontal disease in pregnancy has been associated with an increase in preterm birth and adverse pregnancy outcomes.[14]  However, treatment of periodontal disease in pregnancy has not been shown to improve pregnancy outcomes.[15]  Periodontitis coexisting with bacterial vaginosis is associated with higher vaginal bacterial counts.[16]  Periodontitis in a person with diabetes has been associated with exacerbation of both conditions.[17, 18]  Treatment of periodontitis in persons with type 2 diabetes has improved glycemic control.[19]

In the evolving picture of the global COVID-19 pandemic, it has been observed that preexisting periodontal disease is a risk factor for developing severe diease.[20]

The association of periodontal disease and rheumatoid arthritis (RA) is established. Treatment for RA often improves the periodontitis, but both require treatment concurrently. It is felt that RA predisposes to periodontal disease, but it is not clear if the inverse is true.[21]

Severe periodontal disease, as shown in the image below, may occur.

Chronic gingivitis leads to tooth loss. ANUG may progress into the local soft tissues of the mouth, resulting in noma or cancrum oris, or may spread hematogenously to any other part of the body.

Complications

Gingivitis is not a direct significant threat to the health of a healthy individual, but it can contribute to illness and cause local and systemic complications.

ANUG that progresses to noma is associated with a mortality rate as high as 70% without proper antibiotics and debridement.

The most common complication of chronic gingivitis is progression to periodontal disease and tooth loss. Areas of chronic gingivitis may predispose the individual to the development of odontogenic abscesses by allowing a route of bacterial invasion into the periodontal space from the gingival pocket. ANUG may be locally destructive and may result in local spread of infection into the surrounding tissues (Vincent angina and noma [cancrum oris]). Potential also exists for systemic spread of infection.

Osteomyelitis of alveolar bone may arise but is uncommon.

Any dental procedures involving manipulation that causes bleeding may result in endocarditis. The presence of gingivitis increases this risk by making the gingiva more likely to bleed with simple manipulation (eg, dental scaling). Bacteria containing plaque accumulation in the gingival pockets are in direct proximity to the areas of disrupted gingiva, increasing the likelihood of bacteria escaping into the general circulation.

Good oral hygiene, including brushing and flossing, treats and prevents chronic gingivitis. If flossing is too much of a bother, then plaque-reducing rinses, used daily, have proven benefit.

Studies show electric toothbrushes to be more effective than manual brushes in preventing gingivitis.[22, 23]

Certain toothpastes, both herbal and non-herbal, have additional benefit.

Historical findings depend on whether the patient has chronic gingivitis or ANUG.

• Chronic gingivitis

  • The most common complaint is bleeding gums. The patient usually notices this when toothbrushing or flossing.

  • Bleeding may be associated with eating, especially foods with a hard consistency, such as apples or crusted bread. These foods may rub against gums.

• Acute necrotizing ulcerative gingivitis

  • Apparently spontaneous bleeding or bleeding in response to very minimal local trauma may occur.

  • ANUG also may produce local pain, malaise, and alterations in taste, such as a metallic flavor.

  • ANUG may produce foul breath.

Chronic gingivitis

Patients have minimal physical findings aside from local findings at the dental-gingival margins.

Gingival pockets may be detected with a periodontal probe. However, the pocket depth may be overestimated when periodontitis is present and underestimated in healthy gums.

Mild bleeding from the gum margins may occur with any manipulation.

Acute necrotizing ulcerative gingivitis

Fever, halitosis, marked gingival edema, and ulceration, especially in the interdental papillae, may be present.

A grey pseudomembrane may be present.

Infection may spread to adjacent soft tissues of the mouth, with noticeable erythema, edema, tenderness, and induration of affected areas.

Laboratory testing is not helpful in diagnosing gingivitis.

If systemic disease or toxin exposure is suspected, laboratory tests should be requested.

A smear to identify the causative agent may be helpful.

Imaging studies are not indicated.

Patients with simple chronic gingivitis should be given nonurgent dental referral.

Patients with ANUG should be seen within 24-48 hours for reevaluation because of risk of local or systemic spread of infection.

In addition to antibiotic therapy, physical and mental stressors should be eliminated. Good oral hygiene is mandatory.

Consultation with a dentist is recommended.

In simple chronic gingivitis, emergency department (ED) intervention is not needed.

In ANUG, patients usually only need pain management in the ED.

If signs of systemic infection (eg, fever, sepsis) or progression to gangrenous stomatitis (noma) with soft tissue or bone destruction are present, then patients will need intravenous antibiotics, and possibly imaging of the affected areas, but this complication is exceedingly rare.

Proper oral hygiene (including brushing and flossing) should be stressed. The patient should be referred to a dentist or periodontist.

General measures include the following:

• Remove irritating factors such as plaque, calculus, and faulty dentures

• Use a warm saline rinse

Regular oral hygiene that includes brushing the teeth with a power brush and flossing or using interdental brushes is the best prevention. Although mouth rinses do reduce bacterial counts in test subjects, no clear clinical advantages have been demonstrated.[24, 25, 2]

The use of a power toothbrush with rotating/oscillating motion is better than a manual brush.

Regular dental check-ups are important.

A consensus report on periodontitis and cardiovascular diseases was released by the European Federation of Periodontology and the American Academy of Periodontology in 2020.[26]

In chronic gingivitis, brushing with a fluoride dentifrice will slow disease progression and may help resolution. Most electric toothbrushes have additional benefit over manual brushing. Daily flossing in addition to brushing will reduce plaque and bacterial counts. Recent studies show that brushing followed by rinsing with chlorhexidine or other solutions may have even better results over brushing and flossing.[27, 28] Gum-care–specific preparations that show benefit are available.[29] Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to speed the resolution of inflammation when teeth are being cleaned and scaled to remove plaque.[30, 31]  It has been demonstrated that some herbal formulations may be beneficial in ameliorating periodontal disease.[32, 33]

In patients with ANUG, treatment involves antibiotics, NSAIDs, and topical Xylocaine for pain relief. Saline rinses can help to speed resolution, and oral rinses with a hydrogen peroxide 3% solution also may be of benefit.

Class Summary

These agents are used to eradicate the bacterial infection that is the hallmark of ANUG. In the future, antibiotics also may be used to treat simple chronic gingivitis, but no current evidence exists to justify this practice. Treatment of gingivitis may be warranted if dental surgery is planned.

Penicillin VK (Veetids)

DOC in patients with ANUG who are not allergic to penicillin.

Erythromycin (EES, Ery-Tab, Erythrocin)

Alternative DOC for patients allergic to penicillin.

Minocycline microspheres (Arestin)

Used as an adjunct to scaling and root planing procedures for reduction of pocket depth in patients with adult periodontitis. May be used as part of a periodontal maintenance program that includes good oral hygiene and scaling and root planing.

Doxycycline (Periostat)

Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. However, some studies have shown that doxycycline reduces elevated collagenase activity in gingival crevicular fluid of patients with adult periodontitis. Clinical significance of these findings is not known.

Clindamycin (Cleocin)

Alternative for penicillin-allergic patients, a popular choice for severe infections or those recalcitrant with penicillin.

Class Summary

This is shown to decrease bacterial counts in oral flora. It probably speeds resolution of gingivitis when combined with brushing and flossing.

Chlorhexidine 0.12% oral rinse (PerioGard)

Has bactericidal activity.

Class Summary

Patients with ANUG should be given a strong analgesic along with topical anesthetics and NSAIDs because pain control is very important in allowing the patient to eat and carry out toothbrushing, flossing, and other oral hygiene maneuvers necessary to eradicate the disease. NSAIDs also help to decrease pain. Although effects of NSAIDs in the treatment of pain tend to be patient-specific, ibuprofen usually is the DOC for initial therapy.

Acetaminophen with codeine (Tylenol #3)

Narcotic analgesic well tolerated by most patients; it may induce severe nausea and vomiting in patients particularly sensitive to the drug.

Ibuprofen (Ibuprin, Advil, Motrin)

Used for pain relief and to decrease gingival inflammation. Use with care in patients with history of asthma or peptic ulcer disease.

Class Summary

These agents are helpful in providing pain control, which is very important in allowing the patient to carry out toothbrushing, flossing, and other oral hygiene maneuvers.

Lidocaine anesthetic

An adjunctive therapy for pain control that decreases the permeability to sodium ions in neuronal membranes. This results in inhibition of depolarization, blocking the transmission of nerve impulses.